AKT1 and infection: Finally, infection with the ΔmiR-UL36/112/148D/Akt shRNA virus demonstrated an enhanced frequency of infectious centers compared to ΔmiR-UL36/112/148D/cel-miR-67 (Fig 8D), but no change in genome copy number (Fig 8E), suggesting that inhibiting Akt in the context of infection with the ΔmiR-UL36/112/148D mutant is able to partially complement the reactivation defect observed when these miRNAs are lacking during infection.